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- Mitochondrial Dysfunction -
General Information:
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Wikipedia entry:
Dr. Ray Shahelien entry:
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Observations:
Mitochondrial
Dysfunction
See also,
Dr. Sinatra
More posts by Dr.
Newport
Multifunctional Cocktail
Anti-oxidant
trio therapy [?]
Methylene Blue
ALA
Cognisure
Parkinson's Disease
"It
could be that the cells are so depleted of the various substances
they need to make energy inside the cell that the cells don't
recover simply by providing ketone. I learned more about other
disease processes where there is also a problem with energy
production in mitochondria, the organelles inside of the cells
that manufacture ATP (adenosine
triphosphate), the very basic energy that drives the whole
function of the cell. Each cell has hundreds to thousands of
mitochondria."
The
article below talks about research into the role of amyloid-beta
proteins in creating nitric oxide, which then damages the
"powerhouse" of the cell, the mitochondria. Could this be why
neurons then have a problem with glucose metabolism, and why MCTs
help?
I
remember reading another article about how LOW concentrations of
methylene blue may help preserve mitochondrial function: "the drug
slows cellular aging and enhances mitochondrial function". The
concentration is reported to be ridiculously low (meaning, more
research into the original paper is warranted.) But, if it is true
that very dilute methylene blue solutions are beneficial, then I
have an "act of desperation" option: Kordon's 2.3% Methylene Blue
solution... for fish! If a "very low concentration -- about the
equivalent of a few raindrops in four Olympic-sized swimming pools
of water" would be effective, then what about a drop of fish
aquarium methylene blue in a gallon or five of drinking water?
But even
if you were to decide on going with laboratory-grade MB, which is
a bit pricey, at this level of concentration, a small quantity of
MB would last years.
Here are
the articles:
Alzheimer's
Disease Linked To Mitochondrial Damage
ScienceDaily
(Apr.
2, 2009)
Investigators
at
Burnham
Institute
for
Medical
Research
(Burnham)
have
demonstrated
that
attacks
on
the
mitochondrial
protein
Drp1
by
the
free
radical
nitric
oxide—which
causes
a
chemical
reaction
called
S-nitrosylation—mediates
neurodegeneration
associated
with
Alzheimer's
disease.
Prior
to
this
study,
the
mechanism
by
which
beta-amyloid
protein
caused
synaptic
damage
to
neurons
in
Alzheimer's
disease
was
unknown...
These
findings
suggest
that
preventing
S-nitrosylation
of
Drp1
may
reduce
or
even
prevent
neurodegeneration
in
Alzheimer's
patients.
The
paper
was
published
in
the
April
3
issue
of
the
journal
Science...
The
team
of
scientists,
led
by
neuroscientist
and
clinical
neurologist
Stuart
A.
Lipton,
M.D.,
Ph.D.,
director
of
the
Del
E.
Webb
Center
for
Neuroscience,
Aging
and
Stem
Cell
Research,
showed
that
S-nitrosylated
Drp1
(SNO-Drp1)
facilitates
mitochondrial
fragmentation,
damaging
regions
of
nerve
cell
communication
called
synapses.
Mitochondria
are
the
energy
storehouses
of
the cell, and their compromise by excessive fragmentation causes
synaptic injury and eventual nerve cell death. Synapses are
critical for learning and memory and their impairment leads to the
dementia seen in Alzheimer's patients...
http://www.sciencedaily.com/releases/2009/04/090402143453.htm
Interesting research suggests that maybe "free radicals" may not
be as big of a problem...
Free
Radicals Good for You? Banned Herbicide Makes Worms Live
Longer
ScienceDaily
(Dec.
20, 2010) — It sounds like science fiction – Dr. Siegfried
Hekimi and his student Dr Wen Yang, researchers at McGill’s
Department of Biology, tested the current “free radical theory
of aging” by creating mutant worms that had increased production
of free radicals, predicting they would be short-lived. But they
lived even longer than regular worms! Moreover, their enhanced
longevity was abolished when they were treated with antioxidants
such as vitamin C...
http://www.sciencedaily.com/releases/2010/12/101220084442.htm
Methylene blue...
Potential
Alzheimer's,
Parkinson's Cure Found In Century-old Drug
ScienceDaily
(Aug.
18, 2008)
A new
study conducted by researchers at Children's Hospital &
Research Center Oakland shows that a century-old drug, methylene
blue, may be able to slow or even cure Alzheimer's and
Parkinson's disease. Used at a very low concentration – about
the equivalent of a few raindrops in four Olympic-sized swimming
pools of water – the drug slows cellular aging and enhances
mitochondrial function, potentially allowing those with the
diseases to live longer, healthier lives.
Methylene
blue,
first discovered in 1891, is now used to treat
methemoglobinemia, a blood disorder. But because high
concentrations of methylene blue were known to damage the brain,
no one thought to experiment with low concentrations. Also,
drugs such as methylene blue do not easily reach the brain...
http://www.sciencedaily.com/releases/2008/08/080818101335.htm
This also begs the question, as I've stated before, that if such
an unimaginably small concentration of MB can be beneficial, can
comparatively dilute solutions of other chemicals in our water,
food, or environment be harmful?
Another point I would like to make is that there are steps to the
disease process. All of these things we have discussed appear to
interrupt different stages. So even if low-concentration MB is
effective, other steps of the disease process, once set in motion,
may still progress. I'm thinking of this in relation to why
attacking the amyloid beta plaque problem doesn't seem too
effective. Perhaps it really is, in the long term, or if the
therapy was started early enough before symptoms appeared. But
once symptoms appear, there is a whole freight train of other ones
in motion. So, snipping off the locomotive without activating the
breaks on the box cars means that the train will keep rolling on
and on for a long, long time.
Early
Role of Mitochondria in Alzheimer's Disease May Help Explain
Limitations to Current Beta Amyloid Hypothesis
ScienceDaily
(Oct.
13, 2010) — Before Alzheimer's patients experience memory loss,
the brain's neurons have already suffered harm for years... A
new study in mouse models by researchers at Columbia University
Medical Center has found that the brain's mitochondria -- the
powerhouses of the cell -- are one of the earliest casualties of
the disease. The study, which appeared in the online Early
Edition of PNAS, also found that impaired mitochondria then
injure the neurons' synapses, which are necessary for normal
brain function.
"The
damage to synapses is one of the earliest events in Alzheimer's
disease, but we haven't been able to work out the events that
lead to the damage. Our new findings, along with previous
research, suggest that mitochondrial changes harm the synapses,
and that we may be able to slow down Alzheimer's at a very early
stage by improving mitochondrial function."
Drugs
that restore mitochondria function may be able to treat
Alzheimer's disease in its earliest stages. One potential drug,
cyclosporin, is already
used in organ transplant and autoimmune patients. Cyclosporin
suppresses the immune system, but it also blocks amyloid beta (Aβ) peptides-induced
mitochondrial injury, Dr. Yan has found in previous
studies (Du et al. Nature Medicine, 2008).
Cyclosporin,
however,
has too many toxic side effects for long term use in other
patients...
Most
Alzheimer's researchers initially believed that Aβ peptides
caused the disease after aggregating together in large,
extracellular plaques, a defining feature of
Alzheimer's-affected brains. But Dr.Yan's findings, along with
those of many other scientists, now point to an earlier role for
Aβ peptides inside the brain's neurons.
The
mitochondria are damaged, the researchers found, when (Aβ)
peptides breach the mitochondria's walls and accumulate on the
inside. Even low concentrations of Aβ peptides, equivalent to
the levels found in cells years before symptoms appear, impair
the mitochondria, particularly mitochondria that supply power to
the neuron's synapses.
When
filled with Aβ peptides, these synaptic mitochondria were unable
to travel down the neurons' long axons to reach, and fuel, the
synapse. And the mitochondria that did make the journey failed
to provide adequate energy to operate the synapses. Without
operating synapses, neurons are unable to function.
"Since
cyclosporin is already FDA approved for use in organ transplant
and autoimmune patients, this research has the potential to lead
to more rapid clinical trials and progress quickly," said Dr.
Yan...
http://www.sciencedaily.com/releases/2010/10/101013122557.htm
In
Parkinson's Disease, Brain Cells Abandon Mitochondria
ScienceDaily
(Oct.
8, 2010) — In a study that sheds new light on the causes of
Parkinson's disease, researchers report that brain cells in
Parkinson's patients abandon their energy-producing machinery,
the mitochondria. A shutdown in fuel can have devastating
effects on brain cells, which consume roughly 20 percent of the
body's energy despite making up only 2 percent of body weight...
researchers, now show that a root cause of Parkinson's disease
may lie in 10 gene sets related to energy production that spur
neurons in the brain to "divorce" their mitochondria and related
energy-producing pathways..."The most exciting result from our
study for me is the discovery of PGC-1alpha as a new therapeutic
target for early intervention in Parkinson's disease. PGC-1alpha
is a master switch that activates hundreds of mitochondrial
genes, including many of those needed to maintain and repair the
power plants in the mitochondria,"... FDA-approved medications [Actos, CoQ10] that activate
that PGC-1alpha are already available for widespread diseases
like diabetes. These medications may jumpstart the development
of new Parkinson's drugs; instead of having to start from
scratch, pharmaceutical companies may be able to dust off their
drug libraries and find look-alike drugs capable of targeting
PGC-1alpha in the brain. "As we wrap up our first year of
publishing the journal, the new study from Zheng et al.
exemplifies the goal of Science Translational Medicine, applying
knowledge and technology from different fields-such as
neuroscience, genomics and bioinformatics-to achieve new
discoveries,"...
http://www.sciencedaily.com/releases/2010/10/101006151557.htm
[See also Medium
Chain Triglycerides (MCT oils) and Glucose Metabolism]
Brain Might Be Key to Leptin's
Actions Against Type 1 Diabetes, Researchers Find
ScienceDaily (Nov. 14, 2010)
New findings by UT Southwestern Medical Center researchers
suggest a novel role for the brain in mediating beneficial
actions of the hormone leptin in type 1 diabetes... They found
that infusing leptin into the lateral ventricle of the animals'
brains reversed the lethal consequences of type 1 diabetes. The
results establish the brain as a potentially critical site for
mediating the metabolism-improving actions of leptin,...
http://www.sciencedaily.com/releases/2010/10/101019171711.htm
As
mentioned earlier, one inherits their mitochondria from their mothers...
Alzheimer's Disease Inherited
Through Maternal Line, Study Finds
ScienceDaily (Nov. 15, 2010)
"Our data indicate that adult children of mothers with
Alzheimer's may be at increased risk for developing the
disease. It is therefore extremely important to understand
the genetic mechanisms involved in maternal transmission of
Alzheimer's disease, which are currently unknown. Identifying a
genetic predictor for the disease might lead to preventive
treatments years before the onset of clinical symptoms."
http://www.sciencedaily.com/releases/2010/11/101115111007.htm
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Preface Brain Failure Notes Notes II
References pg. 1 References pg. 2
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Updated: July 2, 2012
Inception: July 2, 2012